^To my understanding, in this sense Methylphenidates (Concerta, Ritalin, Focalin XR, etc) are probably a bit better in that they seem to lack the potential for neurotoxicity because they only act as NDRIs without the neurotransmitter cell entrance 'releasing' potential.
I think the key point here. Is that methylphenidate acts as a norepinephrine-dopamine reuptake inhibitor. Methylphenidate is most active at modulating levels of dopamine and to a lesser extent noradrenaline. It shares the similar qualities with the amphetamine class with it's affinity to bind to DAD and NET.
The big difference is the sheer magnitude of the amphetamine to not only bind to the transporters but to such a severe degree. Amphetamines are a rare breed in that they are extremely,. Inhibiting not only the functioning aggressive competitive inhibitors. Inhibiting not only the normal function of DA and NE transport. But goes many steps further by entering the s of the neuron and stops the complete normal functioning VMAT and the proton pump by it's aggressive, complete inhibiting nature. The result not only forces the overwhelming influx of the intercellular DA into the presynaptic vesicles. This extreme concentration of DA. New channels are formed in the presynaptic area to release the buildup and dump the DA out. The combination of DA overload flooding the neuron and the strangle hold of the amphetamine on the DAT. The extreme malfunctioning of the neuronal infrastructure that transports the monomines to the storage vesicles finally creates the complete malfunction of DAT. It now starts pumping the DA into the synapse instead into the neuron.
Moreover, MPH is thought to act as a releasing agent by increasing the release of dopamine and norepinephrine, though to a much lesser extent than amphetamines.Moreover, MPH is thought to act as a releasing agent by increasing the release of dopamine and norepinephrine, though to a much lesser extent than amphetamines.
Where as, MPH is thought to act as a releasing agent by increasing the release of dopamine and norepinephrine to a much lesser extent than amphetamines. Methylphenidate fundamental difference from amphetamines, is that MPH increases the general firing rate. MPH does not reverse the flow of the monoamine transporters.Although methylphenidate can be considered an amphetamine close derivative. Both have a d and l isomer but differences exist in its pharmacology; amphetamine works as a dopamine transport substrate. Methylphenidate works as a dopamine transport blocker.
When talking of the developmental disorder ADHD from a strictly neuropharmacological view; MPH's therapeutic effects concerning ADHD includes blocking the reuptake of dopamine into nerve terminals. It also stimulates the release of dopamine from dopamine nerve terminals. Which increases dopamine levels in the synapse. It's basically a da and NE reuptake inhibitor. Finally, it increases the magnitude of dopamine release after a stimulus, increasing concentration. . The slower acting stimuli of MPH on DA and NT increase tonic firing into the prefrontal cortext. Slow tonic functionitioning of DA and NE reduces both of the neurotransmitters low concentration in the prefrontal cortext.
Other mitigating issues concerning ADHA include genetics, diet, and social enviroments.